Activin A is a
growth factor expressed in the endometrium, where it modulates tissue remodeling and enhances decidualization. The effects of
activin A are counteracted by two
binding proteins, namely
follistatin and
follistatin-like 3 (FSTL3). We have evaluated the effects of
estrogen and
progestin on the endometrial expression of
activin betaA subunit,
follistatin and FSTL3 in ovariectomized rats. Adult female Wistar rats (n = 21) were ovariectomized and received one week later a single dose of
estradiol benzoate (1.5 mg/kg
body weight, i.m. injection), either alone (n = 7) or associated with depot
medroxyprogesterone acetate (3 mg/kg
body weight, i.m. injection, n = 7), or oil vehicle (control group, n = 7). One week later,
activin betaA subunit
mRNA levels had increased significantly in the uteri of rats treated with
estradiol alone (7.4 fold increase over controls, P < 0.05) and to the same extent in rats receiving
estradiol plus
medroxyprogesterone (6.1 fold increase over controls, P < 0.05). This was accompanied by increase of betaA subunit immunostaining in
estradiol and
estroprogestin treated rats, which was noted only in the surface endometrial epithelium.
Follistatin mRNA expression, conversely, showed a significant decrease in the groups treated with
estrogen alone and
estrogen plus
progestin (P < 0.05), and
follistatin immunostaining in the glandular epithelium was weaker in
estradiol and
estroprogestin-treated rats compared to controls. FSTL3 expression was similar in the 3 groups. In conclusion, the expression of
activin betaA subunit increases and that of
follistatin decreases following
estrogen replacement in the endometrium of ovariectomized rats, and these effects are not further altered by the addition of
progestin.